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Central amygdala somatostatin neurons modulate stress-induced sleep-onset insomnia
Sleep-onset insomnia, characterized by difficulty falling asleep, is linked to increased health risks. Previous studies have shown that the central amygdala (CeA) plays a crucial role in stress regulation, with the somatostatin neurons in the CeA (CeASST+) involved in adaptive stress responses. However, the role of CeASST+ neurons in stress-induced sleep-onset insomnia remains unclear. In this study, we found that the activity of CeASST+ neurons is closely associated with stressful events using fiber photometry in mice. Acute optogenetic activation of CeASST+ neurons induced a rapid transition from non-rapid eye movement (NREM) sleep to wakefulness. Semi-chronic optogenetic and chemogenetic activation of CeASST+ neurons led to prolonged sleep-onset latency and increased wakefulness. Chemogenetic inhibition of these neurons ameliorated sleep-onset insomnia induced by stressful stimuli, but did not affect sleep-wake behavior under physiological conditions. Collectively, our results suggested that CeASST+ neurons are a key neural substrate for modulating stress-induced sleep-onset insomnia, without influencing physiological sleep. These findings highlight CeASST+ neurons as a promising target for treating stress-related sleep-onset insomnia in clinical practice.
The association between irregularity in sleep-wake rhythm and CPAP adherence
This study aims to evaluate the association between sleep-wake rhythm regularity and continuous positive airway pressure (CPAP) adherence. We retrospectively analyzed sleep-wake rhythms with activity monitoring and CPAP adherence among obstructive sleep apnea (OSA) patients newly diagnosed and introduced to CPAP therapy at the Sapporo Hanazono Hospital from January 2018 to June 2022. Among a total of 45 patients, 10 withdrew from CPAP therapy within a year. Nineteen were classified into the good-adherence and 16 into the poor-adherence group. No significant differences were detected among the groups in apnea-hypopnea index (AHI), sleep efficiency, or subjective sleep quality, but a difference was observed in sleep latency, with the CPAP withdrawal group showing higher variability in sleep onset and lower regularity and/or amplitude in circadian behavior activity rhythm than the good-adherence group. Our results suggest that irregularities, particularly in sleep onset, and damped sleep-wake rhythm can be risk factors for CPAP withdrawal.
The evolution of preferred male traits, female preference and the G matrix: “Toto, I’ve a feeling we’re not in Kansas anymore”
Female preference exerts selection on male traits. How such preferences affect male traits, how female preferences change and the genetic correlation between male traits and female preference were examined by an experiment in which females were either mated to males they preferred (S lines) or to males chosen at random from the population (R lines). Female preference was predicted to increase the time spent calling by males. Thirteen other song components were measured. Preference for individual traits was greatest for time spent calling(CALL), volume(VOL) and chirp rate(CHIRP) but the major contributors in the multivariate function were CALL and CHIRP, the univariate influence of VOL arising from correlations to these traits. Estimation of β, the standardized selection differential, for CALL resulting from female preference showed that it was under strong direct selection. However, contrary to prediction, CALL did not change over the course of the experiment whereas VOL, CHIRP and other song components did. Simulation of the experiment using the estimated G matrix showed that lack of change in CALL resulted from indirect genetic effects negating direct effects. Changes in song components were largely due to indirect effects. This experiment showed that female preference may exert strong selection on traits but how they respond to such selection will depend greatly upon the G matrix. As predicted, female preference declined in the R lines. The genetic correlations between preference and preferred traits did not decline significantly more in the R lines, suggesting correlations resulted from both linkage disequilibrium and pleiotropy.
Introduction of novel objects to the home cage of mice repeatedly disturbs sleep for seven days with minimal stress induction
The increasing prevalence of low sleep quality is a significant issue, particularly among adolescents, necessitating a deeper understanding of its biological consequences. In sleep research, various protocols are used for sleep deprivation or disturbance, each presenting its own set of confounding factors crucial to consider. We developed a standardized seven-day sleep disturbance protocol using daily four-hour exposures to novel objects to minimize mouse stress. Objects were selected and characterized for their wake-promoting properties, and exposure timing was structured to reduce variability and enhance experimental reliability and reproducibility. During the four hours of sleep disturbance, the mice were efficiently sleep-deprived during each exposure. Thus, the selected objects efficiently kept the mice awake also after seven days exposure. On the first day of sleep disturbance, the protocol induced a sleep deprivation effect when measured over 24 h (hours), but by the seventh day, the mice recovered the sleep loss over the 24 h. Thus, this method induces an acute sleep loss, but over days it induces a sleep disturbance and not a full sleep deprivation. Fecal corticosterone concentrations remained unchanged during the seven days of sleep disturbances, suggesting that voluntary wakefulness is not stressful. Importantly, we show that the mice compensate for their sleep loss during the week of sleep disturbance, highlighting the need for better validation of long-term sleep deprivation protocols in the sleep field to accurately separate sleep deprivation from sleep disturbance.
Mettl3-m6A-NPY axis governing neuron–microglia interaction regulates sleep amount of mice
Sleep behavior is regulated by diverse mechanisms including genetics, neuromodulation and environmental signals. However, it remains completely unknown regarding the roles of epitranscriptomics in regulating sleep behavior. In the present study, we showed that the deficiency of RNA m6A methyltransferase Mettl3 in excitatory neurons specifically induces microglia activation, neuroinflammation and neuronal loss in thalamus of mice. Mettl3 deficiency remarkably disrupts sleep rhythm and reduces the amount of non-rapid eye movement sleep. We also showed that Mettl3 regulates neuropeptide Y (NPY) via m6A modification and Mettl3 conditional knockout (cKO) mice displayed significantly decreased expression of NPY in thalamus. In addition, the dynamic distribution pattern of NPY is observed during wake-sleep cycle in cKO mice. Ectopic expression of Mettl3 and NPY significantly inhibits microglia activation and neuronal loss in thalamus, and restores the disrupted sleep behavior of cKO mice. Collectively, our study has revealed the critical function of Mettl3-m6A-NPY axis in regulating sleep behavior.
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